Frontiers in immunology · 2026
Metabolic dysregulation and antibody-mediated rejection after kidney transplantation: interacting mechanisms and emerging clinical strategies.
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Yang Qizhen, Tang Shuai, Zhu Kejing, Niu Yulin
Аннотация
BACKGROUND: Kidney transplantation (KT) improves survival in end-stage renal disease, but long-term outcomes are undermined by antibody-mediated rejection (ABMR) and metabolic complications. Recent insights suggest a mechanistic interplay between immune injury and metabolic dysregulation.
METHODS: This narrative review synthesizes current literature on the pathogenesis and clinical impact of antibody-mediated rejection (ABMR), the epidemiology of post-transplant metabolic syndrome-including post-transplant diabetes mellitus, dyslipidemia, and hypertension-and their bidirectional relationship. Emerging diagnostic tools and therapeutic strategies are also examined.
RESULTS: ABMR remains a leading cause of late graft failure. Concurrently, 30% ~ 50% of KT recipients develop metabolic syndromes within the first year, driven by immunosuppressive agents and underlying risk factors. Metabolic abnormalities enhance endothelial activation and complement-driven inflammation, aggravating ABMR. Conversely, immunosuppressive intensification to treat ABMR worsens metabolic profiles, forming a vicious cycle. Novel immunologic (e.g., complement inhibitors, anti-CD38 antibodies) and metabolic (e.g., SGLT2 inhibitors, GLP-1 receptor agonists) agents show promise, though data on long-term efficacy remain limited.
CONCLUSION: Integrated immunometabolic strategies are essential for optimizing graft and patient survival. Future research should focus on personalizing immunosuppression and targeting metabolic health to break the feedback loop linking ABMR and metabolic disease.
METHODS: This narrative review synthesizes current literature on the pathogenesis and clinical impact of antibody-mediated rejection (ABMR), the epidemiology of post-transplant metabolic syndrome-including post-transplant diabetes mellitus, dyslipidemia, and hypertension-and their bidirectional relationship. Emerging diagnostic tools and therapeutic strategies are also examined.
RESULTS: ABMR remains a leading cause of late graft failure. Concurrently, 30% ~ 50% of KT recipients develop metabolic syndromes within the first year, driven by immunosuppressive agents and underlying risk factors. Metabolic abnormalities enhance endothelial activation and complement-driven inflammation, aggravating ABMR. Conversely, immunosuppressive intensification to treat ABMR worsens metabolic profiles, forming a vicious cycle. Novel immunologic (e.g., complement inhibitors, anti-CD38 antibodies) and metabolic (e.g., SGLT2 inhibitors, GLP-1 receptor agonists) agents show promise, though data on long-term efficacy remain limited.
CONCLUSION: Integrated immunometabolic strategies are essential for optimizing graft and patient survival. Future research should focus on personalizing immunosuppression and targeting metabolic health to break the feedback loop linking ABMR and metabolic disease.